The 'triple D' mutation in Unc-93 homolog B1 (Unc93b1), an integral component of endoplasmic reticulum, involved in the trafficking of TLR3, TLR7 and TLR9 [55,56], abolishes endosomal TLR signaling [55] and suppresses disease in lupus-prone C57BL/6-Faslpr, BXSB [46] and MRL-Faslpr (Koh YT et al, J. Immunol. This evidence concerns the gene TLR9 and systemic lupus erythematosus.